Abstract

A modified SIR model is used to explain the transmission of Mycobacterium ulcerans (MU) and its dependence on arsenic (As) environments. Some studies have suggested that As plays a major role in the spread and prevalence of buruli ulcer (BU). In addition, it has been hypothesized that a vector in the form of a water-bug plays a key role in the epidemiology of BU. We develop an epidemiological model based on these assumptions for the dynamics and prevalence of BU and show that As positively induces the growth and spread of MU.